Commotio cordis—Latin for “agitation of the heart”—is the second-most common cause of sudden cardiac death in young athletes, especially in baseball, hockey and football players. A single blow to the chest can cause life-threatening cardiac arrhythmias—problems with the rate or rhythm of the heartbeat. The key to understanding commotio cordis may be to model spiral waves of electrical excitation in the heart. The breakup of a spiral wave can lead to sudden cardiac death, but the underlying mechanisms are poorly understood.

In a paper accepted for publication in Physical Review Letters, researchers used a model to identify how a hit to the heart can disrupt its electrical waves, explaining the conditions under which the impact can cause cardiac arrhythmias. “It is one of the most important problems in theoretical cardiology to understand mechanisms of wave break—the break of electrical waves of excitation—in the heart,” said first author Louis Weise of Utrecht University in the Netherlands.

The electrical activity of the heart governs its mechanical pumping. Conversely, the deformation of heart muscle tissue, for example, due to a mechanical impact on the chest, affects cardiac electrophysiology. This inverse process, known as mechano-electrical feedback, or MEF, can either cause or abolish cardiac arrhythmias. “The main motivation of our work is to find out how MEF influences the onset of cardiac arrhythmias,” Weise said.

As a doctoral student in theoretical biology at Utrecht University and later as a postdoctoral fellow in the laboratory of senior author Alexander Panfilov of Ghent University in Belgium, Weise developed mathematical models for cardiac tissue and applied them to study the emergence of spiral waves and cardiac arrhythmias.

In the new study, Weise and Panfilov set out to identify how a mechanical force can disrupt, or break, electrical waves in the heart muscle. Their method combined a model for human cardiac cells with a mechanical model for cardiac tissue. It also incorporated a model for how electrical excitation and muscle contraction are coupled in human cardiac tissue.

“The model used in this study brings together several smaller models of the electrical, mechanical and chemical signals in individual cardiac cells and how these systems interact with each other in a larger cardiac tissue,” said Seth Weinberg, an assistant professor of biomedical engineering at Virginia Commonwealth University. “This level of detail is not often included in most cardiac modeling studies. This allows the authors to study the effect of mechanical impacts on creation or termination of arrhythmias, with a high level of detail, in a way that would not be possible otherwise.”

In the study, the researchers applied an external mechanical load to the model to simulate pressure on the surface of a thin slice of cardiac tissue. They studied how external mechanical loads that varied widely in strength and duration triggered the breakup of spiral waves. This is important because scientists believe the breakup of a spiral wave can cause the heart to go from rapid beating to irregular, rapid beating, or fibrillation. This can lead to sudden cardiac death, which occurs when the heart develops an arrhythmia that causes it to unexpectedly stop beating.

“Our paper illustrates a novel mechanism of wave break due to MEF,” Weise said. “An external mechanical load mimicking a punch on the chest causes acceleration of wave fronts that leads to collision of a wave front with another wave's back, resulting in break. This finding is particularly interesting as it addresses a phenomenon that is known in cardiology for more than 100 years—commotio cordis—when an impact on the chest causes sudden cardiac death.”

Moving forward, the authors will test their mechanism using a whole heart model to make more quantitative predictions on the clinical implications of their findings. They are also reaching out to experimental groups to test their mechanism in cardiac tissue slices, cell cultures or animal models.

In the end, this research could have important clinical implications. “Sudden cardiac death by commotio cordis often occurs from impacts with the chest during sports and other physical activities, for example, a baseball or hockey puck hitting the chest,” said Weinberg. “The predictions in this study could help inform and improve the design of better sports safety equipment, such that chest impacts are less likely to cause a potentially lethal perturbation to the heart.”